I. Androgens and their receptors Benign prostatic hyperplasia is a relatively common disease in the elderly male population, and its main symptom is difficulty in urination, which is what people call lower urinary tract obstruction symptoms. Previously, clinical experience has suggested a relationship between the symptoms of prostate enlargement and bladder outlet obstruction, but this view is now considered too mechanical, too simple, and too subjective. Based on the analysis of the results of various studies over the past decades, no study has yet been able to clarify the causal relationship between the pathological histological manifestations of the prostate and the symptoms of progressive dyspareunia caused by symptoms of lower urinary tract obstruction. Also the extent to which there is a correlation between the obstruction of lower urinary tract drainage, and the diminished function of the patient’s bladder forcing muscles lacks objective studies, because the determination of the function of the forcing muscles is difficult; in addition, the bladder outlet obstruction itself can cause a neurological action of the bladder and impairment of the function of the bladder forcing muscles, which can cause a series of compound symptoms. Androgens, while stimulating cell proliferation and differentiation, can also inhibit apoptosis, as seen in models of prostate enlargement using androgen co-induction, where prostate gland volume increases, but the rate of cell replication and proliferation decreases instead. The androgens entering the prostate are produced mainly in the testes, with a small amount from the adrenal glands, but generally considered to be less than 10%, and the ratio of testosterone, dihydrotestosterone, in peripheral blood, and in prostate tissue, dihydrotestosterone is as high as 80%; its affinity for androgen receptors is much stronger and its biological effects are more potent. Testosterone mainly stimulates normal testicular physiological functions and male muscle growth. After entering the prostate, testosterone is catalyzed by 5-alpha reductase and transformed into dihydrotestosterone, or by aromatase and transformed into estrogen, while dihydrotestosterone acts almost entirely on the prostate, and the process of testosterone catalyzed by 5-alpha reductase is irreversible. Until now, although it can be demonstrated that androgens can increase the volume of prostate glands, there is no evidence that androgens promote mitotic cell division, and only molecular biological evidence that androgen withdrawal can promote apoptosis. Androgen depot treatment has a significant effect on prostate enlargement. After decreasing androgen levels in patients, the patient’s prostate vasculature produces sudden, dramatic and substantial constriction, and this change in vasoactivity is not mediated by vasoactive factors. In elderly patients, androgen levels are reduced in the peripheral blood circulation; however, in the hyperplastic prostate gland, dihydrotestosterone levels are “normal” and androgen receptor levels are significantly higher than normal. Some scholars have studied the changes in penile androgen receptor levels during the growth and development of the normal male penis, and the results show that in developing males, penile androgen receptor levels are higher, while when the male reproductive organs mature, the androgen receptor levels in the peripheral blood circulation are still higher, even higher than during puberty, but the penile body androgen receptors are in a resting state, at which time the male penis stops developing and no longer grows. The penis is no longer growing, but if the androgen receptors are activated, then the male penis can continue to grow. This principle, whether the endocrine mechanism of prostate enlargement has the same explanatory benefit, is worthy of further study, but provides a valuable piece of information for our research at a deeper level. Second, 5-alpha reductase According to current research, 5-alpha reductase is divided into two main types, type 1 and type 2. Its main role is to catalyze the conversion of testosterone to dihydrotestosterone. The type 1 5-alpha reductase is mainly located in tissues and organs other than the prostate, such as the skin and liver, etc. The type 2 5-alpha reductase is mainly found in the prostate glands. It produces dihydrotestosterone which acts in a paracrine mode on prostate parenchyma and interstitial cells. In contrast, dihydrotestosterone in the peripheral circulation acts in a true endocrine mode on other organs of the organism. The deficiency of 5-alpha reductase can lead to a variety of diseases. In patients with male pseudohermaphroditism, which is an autosomal dominant disorder, these patients, although they also have the appearance of male external genital organs, have distinctly masculine feminine features and, throughout their lives, do not develop prostate enlargement or prostate cancer. The most important of the anti-androgenic mechanism of the drugs used to treat prostate enlargement is the antagonism of type 2 5-alpha reductase, which in turn inhibits the production of dihydrotestosterone. The actual testosterone level in the peripheral blood gradually decreases and the estrogen level gradually increases in the male population as they age, however, the dihydrotestosterone and androgen receptors in the prostate tissue are always at a high level. Several studies have shown that prostate volume is negatively correlated with bioactive testosterone volume but positively correlated with the estrogen/bioactive testosterone ratio. Estrogen has both alpha and beta types of receptors, with beta-type estrogen receptors predominating in the glandular cells of the prostate and in the mesenchymal cells, and both receptors exert a regulatory effect on prostate growth simultaneously. Estrogen does not directly promote prostate growth, but on the one hand binds to estrogen receptors and inhibits apoptosis of prostate gland cells and mesenchymal cells; secondly, estrogen increases androgen sensitivity by inducing the production of androgen receptors in prostate glands with an increase in number; and thirdly, estrogen sensitization. α-ER is considered to be the most important pathway by which estrogen regulates prostate growth. Thus, we can see such a peculiar phenomenon in patients with benign prostatic hyperplasia, that is, an imbalance in the ratio of estrogen to androgen, low androgen levels along with high androgen receptor concentration levels, and a combination of factors that lead to the proliferation of prostate gland cells and interstitial cells. This article briefly describes the mechanisms by which steroid hormones promote prostate tissue growth and inhibit prostate cell apoptosis through various pathways, giving us more insight into the molecular biology of the pathogenesis of BPH, and it also provides us with another way of thinking about conservative treatment of prostate hyperplasia, by uniquely correcting the imbalance in the ratio of androgen levels, or by blocking the dihydrotestosterone This is a very good idea, but we need to explore and study further how feasible this idea is and how effective their treatment is.